Serum level of vascular endothelial growth factor in coronary artery disease Egyptian patients with and without diabetes mellitus

ABSTRACT

Coronary collateral blood vessels formation helps to preserve myocardial function in coronary artery disease as their presence reduces the degree of myocardial ischemia and functional deficit. Vascular endothelial growth factor [VEGF] plays a significant role in this adaptive process. Diabetes mellitus decreases the expression of messenger ribodeoxy nucleic acid [mRNA] and protein for VEGF and its receptors in the myocardium, so diabetes mellitus is one of the first negative predictors of collateral vessel formation. The aim of this work is to estimate the level of serum VEGF in a group of non diabetic patients complaining of coronary artery disease and another group of non insulin dependent diabetic patients complaining of coronary artery disease and to evaluate the relation between diabetes mellitus and the level of VEGF in patients complaining of coronary artery disease in comparison to control group and to assess the relation of VEGF level to systolic and diastolic functions of the heart and to resting wall motion abnormalities in ischemic heart disease patients. In this study we measured the serum level of VEGF in 30 non diabetic patients with coronary artery disease, 30 non insulin dependent diabetic patients with coronary artery disease and 20 apparently healthy subjects matched for age and sex using enzyme immunoassay methods. The study revealed that as in non diabetic patients with coronary artery disease, there was a significant increase in the level of serum VEGF while in diabetic patients there was a significant decrease of the serum level of VEGF, so diabetes mellitus is considered a major risk factor for patients with coronary artery disease as it decreases the level of VEGF induced by myocardial ischemia which is very important for the formation of coronary collaterals. This effect was reflected on systolic and diastolic functions and wall motion abnormalities which were more significantly affected in type 2 diabetic patients and could be explained by reduced collateral vessel formation